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doi: 10.1126/science.1232458 26 LueckeSHolleuferAChristensenMHJnssonKLBoniGASrensenLKet al

Mechanisms of hepatic triglyceride accumulation in non-alcoholic fatty liver disease

Your body needs B12 to: Maintain healthy blood cells Protect nerves throughout your body Manufacture DNA Prevent fatigue and weakness Stabilize mood Promote healthy skin, hair and nails Maintain reproductive health You absorb B12 from certain foods via a 2-step process: When was the last time you felt amazing

Heres how they work together: Folates role: Dietary folate converts to 5-MTHF (active folate) via the MTHFR enzyme 5-MTHF donates a methyl group to homocysteine This requires B12 as a cofactor for the enzyme methionine synthase The result: homocysteine converts to methionine B12s role: B12 (as methylcobalamin) acts as a cofactor for methionine synthase It helps transfer the methyl group from 5-MTHF to homocysteine Without adequate B12, folate gets trapped and cant donate its methyl group This is called the methyl trap What happens when one is deficient: Low B12 with adequate folate: Folate cant function properly (methyl trap) Homocysteine rises despite good folate levels Methylation slows down Can mask B12 deficiency symptoms initially Low folate with adequate B12: Not enough methyl groups available for donation Homocysteine rises Methylation impaired DNA synthesis affected Both low: Severe methylation impairment Very high homocysteine Anemia (megaloblastic) Neurological damage risk Why MTHFR mutations affect this partnership: With MTHFR mutations: Your body cant efficiently convert folate to 5-MTHF This creates a bottleneck in the methylation cycle Even with adequate B12, you dont have enough active folate to work with it Result: elevated homocysteine, poor methylation The solution: Bypass the MTHFR bottleneck by taking pre-methylated folate (5-MTHF) that doesnt require conversion

Inflammation, oxidative stress, and fibrosis are intricately associated processes in the etiopathogenesis of CKD [7]